Alzheimer's disease (AD) and idiopathic Parkinson's disease (PD) are characterized by distinctive clinical phenotypes, and by pathological abnormalities in the postmortem brain that are relatively specific for each of these disorders. However, classic PD patients may develop a dementia that resembles AD, and extra-pyramidal signs may emerge in patients with classic AD. Further, characteristic AD lesions such as neurofibrillary tangles (NFTs) and senile plaques (SPs) may be detected in the brains of PD patients with dementia, and the brains of AD patients may contain numerous cortical and subcortical Lewy bodies (LBs). Indeed, demented elderly patients with postmortem evidence of abundant AD lesions and cortical LBs are thought to represent a form of AD known as the LB variant of AD (LBVAD) or AD with diffuse LB disease (DLBD). However, when abundant cortical LBs alone are detected in elderly demented patients, these patients are assigned a diagnosis of pure DLBD. Finally, phenotypic overlap of AD, PD, the LBVAD and DLBD is common. The consistent assignment of case material to one of several possible diagnostic categories (e.g. PD, AD, DLBD, controls, etc.) is essential for many of the Specific Aims in the subprojects of this Program Project. For this reason, the major goals of the Neuropathology Core are to harvest, preserve, store and thoroughly characterize postmortem tissues from patients followed in the clinical core who die and have consented to an autopsy. Based on the neuropathological examination, the cases will be assigned to a defined diagnostic category such that well characterized and optimally preserved tissue samples can be distributed to the Project investigators. All information on this case material (e.g. age of the patient, diagnosis, postmortem interval, means of tissue denaturation, tissue recipients, etc.) will continue to be entered into a data base which will be used as a research tool by investigators in the Cores and Projects. Special attention will be given to correlative studies that might clarify the role of the Apoliprotein E genotype as a risk factor in LB disorders, and the contributions of cortical LBs to the dementia in the LBVAD, DLBD and in PD patients who lack cortical pathology other than LBs.